Intercellular adhesion molecule-1 (ICAM-I) is a cytokine-inducible adhesion molecule expressed on cells of multiple lineages at sites of inflammation. See, e.g., Vejlsgaard et al, J. Amer. Acad. Demtol. 20: 782 (1989) and Sobel et al, Am. J. Pathol. 136: 1309 (1990). It is a ligand for at least 2 members of the CD18 family of leukocyte adhesion molecules (LFA-1 and Mac-1) and mediates, in part, granulocyte extravasation, lymphocyte mediated cytotoxicity and the development of specific immunological responses involving cell-cell interactions. See, e.g., Springer, T. A., Nature 346: 425 (1990). Antibodies to ICAM-1 have been shown to inhibit leukocyte adhesion to endothelial cells, granulocyte migration through endothelium, mitogen and antigen induced lymphocyte proliferation and mixed lymphocyte reactions in vitro. See, e.g., Smith et al, J. Clin. Invest. 82: 813 (1987). In vivo, antibodies to ICAM-1 inhibit neutrophil trafficking into inflamed lungs in rabbits, nonhuman primate kidney and heart allograft refection, and antigen induced airway eosinophil influx and airway hyperresponsiveness. See, e.g., Barton et al, J. Immunol. 143: 1278 (1989). Structurally, ICAM-1 is a member of the immunoglobulin supergene family with 5 immunoglobulin-like domains, a single transmembrane region and a short cytoplasmic tail. See, e.g., Staunton et al, Cell 52: 925 (1988). ICAM-1 has been identified as a receptor for the major rhinovirus group and a genetically engineered form of ICAM-1 lacking the cytoplasmic tail and transmembrane region has been shown to inhibit rhinovirus infection in vitro. Marlin et al, Nature 344: 70 (1990) (hereinafter referred to as "Marlin et al"), herein incorporated by reference.
It is the purpose of this invention to provide a method for the detection of inflammation in a patient by measuring the amount of a soluble form of ICAM-1 in circulation (cICAM-1) in the bodily fluids of the patient.